xxx red flag for EYE xxx if you have time Flashcards

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1
Q

what are the red flags for eye examination ?

A

eye pain moderate to severe

photophobia

visual disturbances - sudden and persistent visual loss for more than 60 minutes

red eye

trauma

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2
Q

what causes the red flag for eye pain ?

A

acute close angled glaucoma

uveitis

aggressive keratitis

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3
Q

what causes the red flag for photophobia ?

A

corneal diseases - bacterial keratitis

anterior uveitis

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4
Q

what causes the red flag for visual disturbances ?

A

persistent visual loss that lasts for more than 24 hours

sudden painful loss :
vascularity problem - retinal vein and artery occlusion
temporal arteritis - anterior ischemic optic neuropathy
stroke affecting visual pathway
vitreous hemorrhage
wet age related macular degeneration
retinal detachment

gradual painless loss :
cataracts 
refractive error 
dry age related macular degeneration 
open angle glaucoma 
tumors affecting visual pathway 
nutritional optic neuropathy 
painful loss
acute close angles glaucoma 
optic neuritis 
temporal arteritis - involves headache rather than eye pain - anterioir ischemic optic neuropathy 
uveitis 
keratitis endophthalmitis 

===========
transient visual loss - lasting less than 24 hours
migraine - typically only one hemifield
amaurosis fugal - profound vision loss in one eye caused by vasculitis or vascular disease
papilloedema

==========

Vision loss due to a functional neurological disorder.

the person has physical symptoms that no medical condition, physical examination or testing can explain.not caused by a physical neurological disease or disorder

is a common presentation, although it should always be a diagnosis of exclusion. It is more common in teenagers and often related to underlying stress and anxiety.
ntermittent blurred vision sometimes with brow ache and photophobia are common, however, complete loss of vision and double vision are also well-recognised presentations.

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5
Q

whenever exploring eye PAIN or any type of PAIN what do you use ?

A

SOCRATES

site - where is the pain

onset - how did the pain start , suddenly or gradually / what were you doing when the pain started
did the pain wake you from sleep

character of the pain

radiation

associated symptoms - nausea , vomitting ,

time course -
how has the pain changed over time
does pain come and go

exacerbating or relieving factors

severity
on a scale one to ten how severe is the pain 10 being the highest

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6
Q

what is the epidemiology of temporal arteritis / giant cell arteries ?

A

females more

70 or more peak incidence

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7
Q

what is the aetiology of temporal arteritis/ giant cell arteries ?

A

genetic predispostion
VIRAL - parvovirus B19
POLYMYALGIA RHEUMATICA - 50 percent of patient with giant cell arteritis have polymyalgia rheumatica

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8
Q

what is the clinical features of giant cell arteritis / temporal arteritis ?

A

fever , weight loss, night sweats
mainly of SHOULDER and HIP joints - myalgia and arthralgia

arterial inflammation - extrocranial branches of the common carotid , internal carrots and external carotid - temporal artery most affected
-NEW ONSET UNILATERAL/BILATERAL headache
pulse synchronous throbbing
typically located over the temples

  • hardened and tender temporal artery

JAW claudication - pain when chewing

VISION LOSS - due to inflammation and occlusion of the ophthalmic artery
= SCINTILLATING SCOTOMA - arch-shaped area of decreased vision that starts centrally and shifts peripherally.
Amaurosis fugax or permanent loss of vision - is a painless temporary loss of vision in one or both eyes. (anterioir ischemic optic neuropathy)

diplopia - due to ischemia of the extraoccular muscle , occulomtor nerves or brain stem

======

large vessels giant cell arteritis : INVOLVES THE AORTA AND PRIMARY BRANCHES 
- angina pectoris
acute coronary syndrome 
limb claudication 
asymmetrical pulses and BP
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9
Q

what is the epidemiology of polymyalgia rheumatica

A

females

most common rheumatic disease f elderly onset over 70 years old

northern europe descent

ASSOCITED WITH GIANT CELL ARTERITIS

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10
Q

what are the clinical features of polymyaglia rheumatica ?

A

fever , weight loss , night sweats
fatigue

musculoskeletal :primarily affects shoulders , neck , pelvic girdle
symmetric pain , worst at night
morning stiffness >45 mins

muscular atrophy not caused by PMR but reduced activity

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11
Q

what is the diagnosis of giant cell arteritis ? and PMR?

A

inflammatory markers - ESR and CRP high

gold standard - TEMPORAL ARTERY BIOPSY

duplex ultrasound - halo sign
non compressible artery with the ultrasound probe
stenotic and occlusive

suspected cranial and extrocranial involvement - high resolution MRI / CTA / FDG-PET

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12
Q

what is the clinical criteria to difffrentiate GCA from other forms of vasculitis ?

A

NOT USED TO DIAGNOSE GCA

patient features - new onset headache 
aged over 50 
temporal artery discrepancies - decreased pulsation or tenderness 
histopathological abnormalities 
elevated ESR 

score 3 or more = GCA likely - investigate
<3 - dd of GCA

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13
Q

some dd of GCA ?

A

polymyalgia rheumatica

vasculitides
takayasu arteritis
polyarteritis nodosa

monocular vision loss
retinal vein occlusion

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14
Q

what is the treatmnet of GCA ?

A

NICE guidelines
new visulaloss - assessment of an ophthalmologist whilst waiting - one - off high dose corticosteroids

INITITAE HIGH DOSE INDUCTION GLUCOCORTICOID THERAPY BEFORE DIAGNSTIC WORK UP OF tabIF CLINICAL SUSPICION TO MINIMISE THE RISK OF complication sushi as vision loss and stroke - IMMEDIATE ADMINISTRATION IS IMPORTNAT TO LOWER THE RISK OF PERMANANT VISION LOSS

acute or intermittent visual loss - IV glucocorticoid therapy
or 60-100mg oral prednisolone for 3 days

suspected GCA without visual symptoms- immediately treated with - 40-60mg oral prednisolone

ischemic organ damage - initial pulse therapy with methylprednisolone 0.25-1g /24

response to corticosteroids is usually rapid - if repose to prednisolone is poor - alternative diagnosis
treatment reduced slowly over several months
FOR 2-4 WEEKS

======
maintenance - taper glucostricoids

glucocorticoid sparing therapy - who relapse or high risk of complication from long term glucocorticoid
tocilizumab -
methotrexate

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15
Q

what is the complication of temporal arteritis / giant cell arteritis ?

A

permanent vision loss if left untreated

cerebral ischemia

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16
Q

what is acute close angled glaucoma ?

A

sudden sharp increase in intraoccqular pressure due to obstruction commonly in the iridocorneal angle

17
Q

what is the etiology of acute and chronic close angled glaucoma ?

A

acute
caused by eye injury - adherence of the iris to the trabecular mesh work
mydriasis - drug induced - - anti cholinergic - atropine
darkness - at night pupil dilate
stress or fear

chronic -
anatomic features - shallow anterioir chamber
age high
asian or inuit ethnicity

18
Q

what are the clinical symptoms of acute angle closure glaucoma

and chronic

A

sudden onset
unilateral inflamed , red , severely painful eye on palpation
frontal headache
blurred vision , HALOS SEEN AROUND LIGHT
mid dilated , irregular , unresponsive pupil
cloudy cornea
EMERGENCY!!!!! - can cause permanent vision loss

chronic
asymptomatic
progressive vision loss
Caused by acute inflammatory conditions of the iris or prolonged apposition between the structures (e.g., uveitis - peripheral anterioir synechiae

19
Q

what is the diagnosis of acute angle closure glaucoma ?

A

acute - emergencyy opthalmic evaluation
confirmed on TONOMETRY elevated intraocular pressure

GONIOSCOPY (GOLD STANDARD) or slit lamp - narrowing or closure of iridocorneal angle

glaucomatous damage performed in all patients- optic disc change - direct fundoscopy
visual acuity
visual field testing

DO NOT USE MUYDRIATIC DRUGS - ATROPINE EPINEPHRINE
and NO DARKNESS FOR EYE TEST - INCREASING MYDRIASIS

20
Q

IF DIAGNOSTIC FINDINGS ARE inconclusive for angle closure glaucoma what are the DD ?

A

painful red eye - uveitis

headache with ocular pain - migraine

21
Q

what is the management of acute closure glaucoma ?

A

EMERGENCY OPTHALMOLGY CONSULTATION
place patient in supine position - moves len slightly posterioir - opens up the iridiocorneal angle
analgesics

IOP decreasing medication
eyedrops direct parasympathomemtic drug - PILOCARPINE 2 PERCENT
pilocarpine may be ineffective because of iris ischemia. It should still be administered, however, because once the IOP decreases as a result of other agents, the iris becomes responsive to pilocarpine

/ ALPHA 2 AGONIST - apraclonidine

/ timolol - beta blocker (avoid in copd , asthmatic , decompensated heart failure , AV block

PLUS

systemic carbonic anhydrase inhibitor (avoided in pregnancy)
ACETZOLOMIDE (avoid in renal insufficiency) 125–250 mg PO every 6 hours

======
vision threatening IOP refectory to medical therapy - anterioir chamber paracentesis
however patient will later on require laser peripheral iridotomy

=====
Standard of care for acute angle-closure glaucoma as soon as the acute attack is resolved and the cornea becomes clear = Laser peripheral iridotomy

Laser peripheral iridoplasty (gonioplasty)
Indication: persistently elevated IOP despite a patent LPI

Surgical peripheral iridectomy
Indication: an alternative to LP iridectomy in patients with acute/chronic angle-closure glaucoma with pupillary block

22
Q

what is the complication of acute angle clusire glaucoma ?

A

rapid permanent vision loss - ischemia and atrophy of optic nerve

23
Q

what is the treatmnet for chronic primary angle closure glaucoma ?

A

laser peripheral iridotomy or open surgery iridectomy prevent progression of glaucomatous optic neuropathy

maintenance pharmacotherapy if elevated top despite iridotomy